AJP - Regulatory, Integrative and Comparative Physiology, Vol 249, Issue 6 781-R786, Copyright © 1985 by American Physiological Society
Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR
R. W. Lappe, J. A. Todt and R. L. Wendt
Previous studies have demonstrated that infusion of synthetic atriopeptin
II (AP II) lowered arterial pressure, reduced regional blood flow, and
increased total peripheral and regional vascular resistances in conscious
spontaneously hypertensive rats (SHR). This study was designed to examine
the mechanism(s) involved in regional vasoconstrictor responses to AP II.
In these experiments, hemodynamic actions of AP II were examined in
control, 6-hydroxydopamine-treated (chemically sympathectomized), and
renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1
microgram X kg-1 X min-1) caused similar reductions in mean arterial
pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/-
2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II
infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and
hindquarters (-18 +/- 10%) blood flow and increased regional vascular
resistance in all three beds. Chemical sympathectomy prevented the fall in
renal blood flow (RBF) and significantly abolished the regional
vasoconstrictor responses to AP II infusion. In unilateral renal-denervated
groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but
failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR
increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in
contralateral-innervated kidneys. This study demonstrated that chemical or
surgical destruction of renal sympathetic nerves abolished AP II-induced
increases in RVR. These data further indicate that in conscious SHR the
regional vasoconstrictor responses to AP II infusion appear to be mediated
by increases in sympathetic tone rather than through direct vascular
actions of AP II.
